The pattern-recognition molecule H-ficolin in relation to diabetic kidney disease, mortality, and cardiovascular events in type 1 diabetes

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  • Jakob Appel Østergaard
  • Fanny Jansson Sigfrids, Folkhälsan Institute of Genetics, Folkhälsan Research Center, Helsinki, University of Helsinki, Helsinki University Hospital
  • ,
  • Carol Forsblom, Folkhälsan Institute of Genetics, Folkhälsan Research Center, Helsinki, University of Helsinki, Helsinki University Hospital
  • ,
  • Emma H Dahlström, Folkhälsan Institute of Genetics, Folkhälsan Research Center, Helsinki, University of Helsinki, Helsinki University Hospital
  • ,
  • Lena M Thorn, Folkhälsan Institute of Genetics, Folkhälsan Research Center, Helsinki, University of Helsinki, Helsinki University Hospital
  • ,
  • Valma Harjutsalo, Folkhälsan Institute of Genetics, Folkhälsan Research Center, Helsinki, University of Helsinki, Helsinki University Hospital, National Institute for Health and Welfare, Helsinki, Finland.
  • ,
  • Allan Flyvbjerg, Steno Diabetes Center, Copenhagen
  • ,
  • Steffen Thiel
  • Troels Krarup Hansen
  • Per-Henrik Groop, Folkhälsan Institute of Genetics, Folkhälsan Research Center, Helsinki, University of Helsinki, Helsinki University Hospital, Monash University

H-ficolin recognizes patterns on microorganisms and stressed cells and can activate the lectin pathway of the complement system. We aimed to assess H-ficolin in relation to the progression of diabetic kidney disease (DKD), all-cause mortality, diabetes-related mortality, and cardiovascular events. Event rates per 10-unit H-ficolin-increase were compared in an observational follow-up of 2,410 individuals with type 1 diabetes from the FinnDiane Study. DKD progression occurred in 400 individuals. The unadjusted hazard ratio (HR) for progression was 1.29 (1.18-1.40) and 1.16 (1.05-1.29) after adjustment for diabetes duration, sex, HbA1c, systolic blood pressure, and smoking status. After adding triglycerides to the model, the HR decreased to 1.07 (0.97-1.18). In all, 486 individuals died, including 268 deaths of cardiovascular causes and 192 deaths of complications to diabetes. HRs for all-cause mortality and cardiovascular mortality were 1.13 (1.04-1.22) and 1.05 (0.93-1.17), respectively, in unadjusted analyses. These estimates lost statistical significance in adjusted models. However, the unadjusted HR for diabetes-related mortality was 1.19 (1.05-1.35) and 1.18 (1.02-1.37) with the most stringent adjustment level. Our results, therefore, indicate that H-ficolin predicts diabetes-related mortality, but neither all-cause mortality nor fatal/non-fatal cardiovascular events. Furthermore, H-ficolin is associated with DKD progression, however, not independently of the fully adjusted model.

OriginalsprogEngelsk
Artikelnummer8919
TidsskriftScientific Reports
Vol/bind11
Nummer1
Antal sider9
ISSN2045-2322
DOI
StatusUdgivet - apr. 2021

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